Advances in Cancer Prevention
Open Access

Iron; Redox reactions; Oxidative stress; Reactive oxygen species; Fenton reaction; Iron homeostasis; Neurodegenerative diseases; Cardiovascular diseases; Cancer; Iron chelation therapy

Introduction

Iron is an essential trace element that plays a vital role in various physiological processes, including oxygen transport, DNA synthesis, and cellular respiration [1]. As a key component of hemoglobin, myoglobin, and numerous enzymes, iron is indispensable for maintaining normal cellular function. However, its redox-active nature allows it to participate in electron transfer reactions, particularly in the conversion between ferrous (Fe²⁺) and ferric (Fe³⁺) states. This property, while crucial for metabolic activities, also makes iron a double-edged sword, as it contributes to the generation of reactive oxygen species (ROS) through Fenton and Haber-Weiss reactions [2].

Oxidative stress arises when there is an imbalance between ROS production and the body's antioxidant defense mechanisms [3]. The excess ROS can cause lipid peroxidation, protein oxidation, and DNA damage, leading to cellular dysfunction and apoptosis. Iron-induced oxidative stress has been strongly implicated in the pathogenesis of various diseases, including neurodegenerative disorders such as Alzheimer's and Parkinson's disease, cardiovascular diseases, cancer, and metabolic disorders. Dysregulation of iron homeostasis, whether through iron overload or deficiency, exacerbates oxidative damage, making it a critical factor in disease progression [4].

Given the significance of iron in redox biology and disease mechanisms, understanding the intricate balance between iron metabolism and oxidative stress is essential for developing targeted therapeutic strategies. This paper explores the role of iron in oxidative stress-related diseases, highlighting the biochemical pathways involved and potential interventions, such as iron chelation therapy and antioxidant-based treatments [5].

Discussion

Iron's dual role in cellular metabolism and oxidative stress makes it a critical factor in health and disease. While essential for various biological functions, its ability to undergo redox cycling contributes to oxidative damage when dysregulated. The interplay between iron metabolism, redox reactions, and disease pathology highlights the need for precise regulation of iron homeostasis to prevent oxidative stress-related conditions [6]. 

Iron and Oxidative Stress in Disease Pathogenesis

Iron-induced oxidative stress is central to the development of several chronic diseases. In neurodegenerative disorders, such as Alzheimer’s and Parkinson’s disease, iron accumulation in the brain enhances ROS generation, leading to neuronal damage and neuroinflammation [7]. Studies have shown elevated iron levels in affected brain regions, suggesting a direct role in disease progression. Similarly, in cardiovascular diseases, iron overload contributes to endothelial dysfunction, lipid peroxidation, and atherosclerosis, increasing the risk of heart failure and stroke. Cancer development is also influenced by iron-mediated oxidative stress. Excess iron promotes DNA damage and genomic instability, which can trigger mutations and uncontrolled cell proliferation. Furthermore, tumor cells exhibit altered iron metabolism, utilizing iron for rapid growth and survival. This has led to the exploration of iron-targeting therapies in oncology, including iron chelators and ferroptosis-inducing agents [8].

Iron Regulation and Therapeutic Strategies

Given the pathogenic role of iron in oxidative stress-related diseases, therapeutic strategies targeting iron metabolism have gained attention. Iron chelation therapy, using agents like deferoxamine and deferiprone, helps reduce excess iron and mitigate oxidative damage [9]. Additionally, antioxidants, such as N-acetylcysteine and polyphenols, can neutralize ROS and protect cells from iron-induced damage. Dietary modifications, including controlled iron intake and increased consumption of natural antioxidants, may also contribute to maintaining iron homeostasis. Advancements in biomarker research have improved the detection of iron dysregulation in disease states, enabling early intervention. The development of novel drugs targeting iron-dependent pathways, such as ferroptosis inhibitors, holds promise for future treatments. However, further research is needed to refine these approaches and ensure their efficacy across different diseases [10].

Conclusion

Iron plays a pivotal role in oxidative stress-related diseases, with its redox activity contributing to pathological processes in neurodegeneration, cardiovascular disease, and cancer. Understanding the mechanisms linking iron metabolism and oxidative stress provides opportunities for developing targeted interventions. Future research should focus on optimizing iron chelation strategies, exploring novel antioxidant therapies, and improving early detection methods to mitigate iron-induced oxidative damage effectively.

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